miRNA biogenesis and inherited disorders: clinico-molecular insights

Pelletier, Dylan; Rivera, Bárbara; Fabian, Marc R.; Foulkes, William D.

doi:10.1016/j.tig.2023.01.009

Cited by 16 publications

(9 citation statements)

References 82 publications

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“…We also analyzed the correlation between mFUT8 and the four candidate miRNAs, and we selected miR‐186‐5p as the sponge miRNA for its significant negative correlation with mFUT8 both in TCGA‐LUAD and our LUAD tumor tissues (Figure 5b, c). AGO2 always mediated the circRNAs sponging miRNA and miRNA cleaving target transcripts 28 . The RIP experiment revealed that circFUT8, mFUT8, and miR‐186‐5p were all significantly enriched under the action of anti‐AGO2 (Figure 5d).…”

Section: Resultsmentioning

confidence: 95%

“…AGO2 always mediated the circRNAs sponging miRNA and miRNA cleaving target transcripts. 28 The RIP experiment revealed that circFUT8, mFUT8, and miR‐186‐5p were all significantly enriched under the action of anti‐AGO2 (Figure 5d ). We also constructed the biotin‐probe labeled circFUT8 and mFUT8, respectively, and we performed pulldown assays to identify that both circFUT8 and mFUT8 could directly interact with miR‐186‐5p (Figure 5e, f ).…”

Section: Resultsmentioning

confidence: 97%

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N⁶‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

Dong,

Liang,

Chen

et al. 2023

Thoracic Cancer

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BackgroundLung cancer is the leading cause of cancer related to mortality worldwide, and the main pathological type is lung adenocarcinoma (LUAD). Circular RNAs (circRNAs) have been reported to be modified by N6‐methyladenosine (m6A), which is involved in the progression of diverse tumors. However, the crosstalk between circRNAs and m6A modification has not been well elucidated in LUAD.MethodsMeRIP‐seq and YTHDF2‐RIP‐seq datasets were explored to identify candidate circRNAs modified by YTHDF2. Dual‐luciferase reporter assay, RIP, and rescue assays were performed to explore the relationship between circFUT8 and its parent mRNA of FUT8. In vitro and in vivo experiments were utilized to uncover the function of circFUT8.ResultsIn this study, we identified a novel m6A‐modified circFUT8, derived from exon 3 of FUT8, which was elevated in tumor tissues compared with adjacent noncancerous tissues. The m6A reader YTHDF2 recognized and destabilized circFUT8 in an m6A‐dependent manner. YTHDF2 also combined with the line form of FUT8 (mFUT8), and circFUT8 competitively interacted with YTHDF2, blunting its binding to mFUT8, to stabilize the mRNA level of FUT8. Additionally, circFUT8 sponged miR‐186‐5p to elevate the expression of mFUT8. Finally, we revealed that circFUT8 promoted the malignant progression of LUAD dependent on the oncogenic function of FUT8.ConclusionsThese findings identified a novel m6A‐modified circFUT8 recognized and destabilized by YTHDF2, which competitively interacted with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in LUAD.

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 97%

N⁶‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

Dong,

Liang,

Chen

et al. 2023

Thoracic Cancer

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“…Mutations are also reported both at the somatic and germline level [10,14,33,34]. At germline level, these genes are known to cause at least three distinct genetic syndromes, with clinical manifestations that range from tumor predisposition (DGCR8 and DICER1 germline mutations) to neurodevelopmental disorders (AGO1/2 germline mutations) [35]. Hence, single nucleotide polymorphism (SNP) in DROSHA and DGCR8 genes can affect their structure or expression, resulting in incomplete miRNA processing influencing the expression of the target gene, thereby acting as a risk factor for cancer that will be further discussed [2].…”

Section: Mirnas As Powerful Biomarkers In Cancermentioning

confidence: 99%

Unraveling the Significance of DGCR8 and miRNAs in Thyroid Carcinoma

Rodrigues,

Da Cruz Paula,

Soares

et al. 2024

Cells

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MicroRNAs (miRNAs) act as negative regulators for protein-coding gene expression impacting cell proliferation, differentiation, and survival. These miRNAs are frequently dysregulated in cancer and constitute classes of blood-based biomarkers useful for cancer detection and prognosis definition. In thyroid cancer (TC), the miRNA biogenesis pathway plays a pivotal role in thyroid gland formation, ensuring proper follicle development and hormone production. Several alterations in the miRNA biogenesis genes are reported as a causality for miRNA dysregulation. Mutations in microprocessor component genes are linked to an increased risk of developing TC; in particular, a recurrent mutation affecting DGCR8, the E518K. In this review, we explore these novel findings and resume the current state-of-the-art in miRNAs in thyroid carcinomas.

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“…4f). MicroRNAs restrain the expression of their binding targets in an Ago2-dependent manner, which is a central component of the RNA-mediated silencing complex (24). We further performed an anti-Ago2 RNA immunoprecipitation (RIP) assay to verify this role of miR-141-3p/186-5p.…”

Section: Linc01671 Induces Crc Cells Emt By Regulating Yy1mentioning

confidence: 99%

LncRNA LINC01671/YY1 positive feedback loop induced EMT modulates CCL2 secretion in colorectal cancer to attract M2-like TAM infiltration

Tan,

Wei,

Zhang

et al. 2023

Preprint

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Background Epithelial-mesenchymal transition (EMT) is involved in the interaction between cancer cells and tumor-associated macrophages (TAMs) in the tumor microenvironment (TME), which intimately affects tumorigenicity and metastasis. However, the potential mechanisms of EMT and the understanding of how EMT-programmed cancer cells affect TAMs recruitment and polarization remain further investigation. Methods The expression of LINC01671, miR-141-3p, miR-186-5p, and YY1 in CRC tissues and cells were detected by RT-qPCR. Functions of LINC01671 on cancer cell proliferation, migration, invasion and EMT were examined by a series of in vitro assays. The underlying mechanism of LINC01671 was investigated by bioinformatics analysis, RNA pull-down, luciferase reporter, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation assays. A co-culture assay in vitro was used to detect the effect of LINC01671 on macrophage recruitment and polarization in TME. A xenograft mouse model was performed to explore the role of LINC01671 on tumorigenicity and TAM polarization. Results LncRNA LINC01671 was significantly overexpressed in colorectal cancer (CRC) tissues, and high LINC01671 level was positively correlated with poor prognosis in CRC patients. Elevated LINC01671 promoted CRC cells proliferation, migration, invasion and EMT in vitro as well as tumor growth and metastasis in vivo. Mechanistically, LINC01671 served as a sponge for miR-141-3p and miR-186-5p to facilitate YY1 expression, which in turn transcriptionally activated LINC01671 expression. Moreover, LINC01671/YY1 modulated CCL2 secretion during CRC cells EMT and subsequently favored TAMs infiltration and M2-like polarization in TME. Conclusion Our data demonstrate that LINC01671, identified as an oncogene, may play a crucial role in regulating YY1-mediated cancer cell EMT, thereby affecting CCL2-related M2-like TAM recruitment in CRC.

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miRNA biogenesis and inherited disorders: clinico-molecular insights

Cited by 16 publications

References 82 publications

N⁶‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

N⁶‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

Unraveling the Significance of DGCR8 and miRNAs in Thyroid Carcinoma

LncRNA LINC01671/YY1 positive feedback loop induced EMT modulates CCL2 secretion in colorectal cancer to attract M2-like TAM infiltration

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miRNA biogenesis and inherited disorders: clinico-molecular insights

Cited by 16 publications

References 82 publications

N6‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

N6‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

Unraveling the Significance of DGCR8 and miRNAs in Thyroid Carcinoma

LncRNA LINC01671/YY1 positive feedback loop induced EMT modulates CCL2 secretion in colorectal cancer to attract M2-like TAM infiltration

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N⁶‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma

N⁶‐methyladenosine‐modified circFUT8 competitively interacts with YTHDF2 and miR‐186‐5p to stabilize FUT8 mRNA to promote malignant progression in lung adenocarcinoma